The general notion is
that deposition of beta-amyloid (Aβ) peptides in senile plaques is the
characteristic feature of the Alzheimer's disease progression. In a recent
study it was found that Pinocembrin may
be a useful drug in the treatment of Alzheimer's disease.
The actual etiology of
Alzheimer's disease is not clearly known and is still debatable.
However it is widely
believed that 'the accumulation of beta-amyloid (Aβ) peptides in the senile
plaques is one of the hallmarks of the progression of the disease.'
degeneration associated with Alzheimer's disease (AD) is affected by
interaction between Aβ and a receptor called receptor for advanced glycation
end products (RAGE).
'Pinocembrin is a
flavanone, a type of flavonoid. It is an antioxidant found in damiana, honey,
Rui Liu et al
published a study in BMC Medicine 2012
based on their findings that pinocembrin protects against beta-amyloid-induced
toxicity in neurons through inhibiting receptor for advanced glycation end
promoting biological activities are attributed to the presence of pinocembrin.
Earlier researches have revealed the neuroprotective effects of pinocembrin
particularly in cases of vascular and ischemic dementia in animals.
Since State Food and
Drug Administration of China approved pinocembrin for being used in stroke
patients, it has been examined for improving cognitive functions and neuronal
protection against toxicity induced by Aβ.
For the purpose of
study, pinocembrin was administrated orally in a dose of 20 mg/kg/day and 40
mg/kg/day for 8 days in mice treated with Aβ 25-35
Alzheimer-like changes. Brain changes were evaluated based on analysis of
neuronal degeneration, behavioral performance and cerebral cortex neuropil
ultrastructure, and RAGE expression.
discovered that pinocembrin, if administered orally, can improve cognitive
function and decrease the neurodegeneration of cerebral cortex in Aβ 25-35
mice. Pinocembrin remarkably reduced the upregulation of receptor for advanced
glycation end products (RAGE). It also reduced the inflammatory response
consequent of Aβ-RAGE interaction.
improved dysfunctioning of mitochondria by enhancing mitochondrial potential
and reducing oxidative stress of mitochondria.
concluded that pinocembrin improved neuronal protection and may prove to be an
important candidate for treating Alzheimer's disease.
Pinocembrin protects against
beta-amyloid-induced toxicity in neurons through inhibiting receptor for
advanced glycation end products (RAGE)-independent signaling pathways and
regulating mitochondrion-mediated apoptosis; Rui Liu et al; BMC Medicine 2012